ArticlePloS one2015
SMAD-independent down-regulation of caveolin-1 by TGF-β: effects on proliferation and survival of myofibroblasts.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 47 citations in OpenAlex.
- Article
- The Inflammatory Nexus of Bronchopulmonary Dysplasia: From Molecular Pathways to Precision Therapeutics.Mediators of inflammation · 2026Review
- O-GlcNAc regulates anti-fibrotic genes in lung fibroblasts through EZH2.Journal of cellular and molecular medicine · 2024Article
- Fibroblasts in rheumatoid arthritis: novel roles in joint inflammation and beyond.Frontiers in medicine · 2024Review
- The uPA/uPAR System Orchestrates the Inflammatory Response, Vascular Homeostasis, and Immune System in Fibrosis Progression.International journal of molecular sciences · 2023Review
- Asiaticoside Combined With Carbon Ion Implantation to Improve the Biocompatibility of Silicone Rubber and to Reduce the Risk of Capsule Contracture.Frontiers in bioengineering and biotechnology · 2022Article
- Noncoding RNAs as Promising Diagnostic Biomarkers and Therapeutic Targets in Intestinal Fibrosis of Crohn's Disease: The Path From Bench to Bedside.Inflammatory bowel diseases · 2021Review
- Anti-Fibrosis Effects of Magnesium Lithospermate B in Experimental Pulmonary Fibrosis: By Inhibiting TGF-βRI/Smad Signaling.Molecules (Basel, Switzerland) · 2021Article
- Fibrostenotic strictures in Crohn's disease.Intestinal research · 2020Review
- Brd4-p300 inhibition downregulates Nox4 and accelerates lung fibrosis resolution in aged mice.JCI insight · 2020Article
- MeCP2 epigenetically regulates alpha-smooth muscle actin in human lung fibroblasts.Journal of cellular biochemistry · 2020Article
- Article
- Failure to Down-RegulateCells · 2020Article
- Fibroblast Senescence in Idiopathic Pulmonary Fibrosis.Frontiers in cell and developmental biology · 2020Review
- Overview of Crosstalk Between Multiple Factor of Transcytosis in Blood Brain Barrier.Frontiers in neuroscience · 2019Review
- Caveolin-1 as a target in prevention and treatment of hypertrophic scarring.NPJ Regenerative medicine · 2019Review
- Causes of Pulmonary Fibrosis in the Elderly.Medical sciences (Basel, Switzerland) · 2018Review
- Scleroderma fibroblasts suppress angiogenesis via TGF-β/caveolin-1 dependent secretion of pigment epithelium-derived factor.Annals of the rheumatic diseases · 2018Article
- Review
- Unraveling SSc Pathophysiology; The Myofibroblast.Frontiers in immunology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Transforming growth factor-β (TGF-β) mediates growth-inhibitory effects on most target cells via activation of the canonical SMAD signaling pathway. This growth-inhibitory activity may be coupled with cellular differentiation. Our studies demonstrate that TGF-β1 inhibits proliferation of primary, non-transformed human lung fibroblasts in association with the induction of myofibroblast differentiation. Differentiated myofibroblasts maintain the capacity to proliferate in response to exogenous mitogenic stimuli and are resistant to serum deprivation-induced apoptosis. These proliferative and anti-apoptotic properties of myofibroblasts are related, in part, to the down-regulation of caveolin-1 (Cav-1) by TGF-β1. Cav-1 down-regulation is mediated by early activation of p38 MAPK and does not require SMAD signaling. In contrast, myofibroblast differentiation is dependent on activation of the SMAD pathway, but not on p38 MAPK. Thus, combinatorial signaling by TGF-β1 of myofibroblast differentiation and down-regulation of Cav-1 by SMAD and p38 MAPK pathways, respectively, confer proliferative and apoptosis-resistant properties to myofibroblasts. Selective targeting of this SMAD-independent, p38-MAPK/Cav-1-dependent pathway is likely to be effective in the treatment of pathological conditions characterized by TGF-β signaling and myofibroblast activation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.